Evidence map›Paper›PMID 35750765›Full record

ArticleCancer immunology, immunotherapy : CII2023

Circ-HSP90A expedites cell growth, stemness, and immune evasion in non-small cell lung cancer by regulating STAT3 signaling and PD-1/PD-L1 checkpoint.

Jie Lei, Jianfei Zhu, Bengang Hui, Chenghui Jia, Xiaolong Yan, Tao Jiang, Xiaoping Wang

Open access · greenAbstract read
In one paragraph

Article in Cancer immunology, immunotherapy : CII, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
2.8field-weighted citation impact, top 8% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

29 citing papers in PubMed, 36 citations in OpenAlex.

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  9. Circular RNAs: key players in tumor immune evasion.Molecular and cellular biochemistry · 2025
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 2 institutions in 1 country.

Jie Lei *Department of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, No.569 Xinsi Road, Xi'an, 710038, Shaanxi, China.
Jianfei Zhu *Department of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, No.569 Xinsi Road, Xi'an, 710038, Shaanxi, China.
Bengang Hui *Department of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, No.569 Xinsi Road, Xi'an, 710038, Shaanxi, China.
Chenghui JiaDepartment of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, No.569 Xinsi Road, Xi'an, 710038, Shaanxi, China.
Xiaolong YanDepartment of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, No.569 Xinsi Road, Xi'an, 710038, Shaanxi, China.
Tao JiangDepartment of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, No.569 Xinsi Road, Xi'an, 710038, Shaanxi, China. jiangtaochest@163.com.ORCID http://orcid.org/0000-0001-6055-9576
Xiaoping WangDepartment of Thoracic Surgery, The Second Affiliated Hospital of Air Force Medical University, No.569 Xinsi Road, Xi'an, 710038, Shaanxi, China. wxpchest@fmmu.edu.cn.
Air Force Medical University · CNXi'an Medical University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundCircular RNAs (circRNAs) are important participators in tumor progression for their stable structure and high tissue-specific expression. The purpose of this research was to clarify the potential and mechanism of a novel circRNA-circ-HSP90A in non-small cell lung cancer (NSCLC).

methodsBiological potentials of circ-HSP90A in NSCLC were measured by functional assays. Molecular interaction was assessed by bioinformatics analysis and mechanical assays.

resultsResults depicted that circ-HSP90A was cyclization from its host gene heat shock protein 90 alpha (HSP90A) and was up-regulated in NSCLC cells. Circ-HSP90A depletion retarded proliferation, migration, invasion, and immune evasion. Mechanistically, circ-HSP90A recruited ubiquitin specific peptidase 30 (USP30) to stabilize HSP90A and then stimulated the signal transducer and activator of transcription 3 (STAT3) signaling. Meanwhile, circ-HSP90A sponged miR-424-5p to programmed cell death ligand 1 (PD-L1).

conclusionsOur study firstly showed that circ-HSP90A promoted cell growth, stemness, and immune evasion in NSCLC through regulating STAT3 signaling and programmed cell death 1 (PD-1)/PD-L1 checkpoint, mirroring that targeting circ-HSP90A might become a novel target of immunotherapy in NSCLC.

Indexed as

Carcinoma, Non-Small-Cell LungLung NeoplasmsMicroRNAsRNA, CircularSTAT3 Transcription FactorApoptosisB7-H1 AntigenCell ProliferationHumansImmune EvasionLigandsMitochondrial ProteinsProgrammed Cell Death 1 ReceptorThiolester HydrolasesB7-H1 AntigenLigandsMicroRNAsMitochondrial ProteinsProgrammed Cell Death 1 ReceptorRNA, CircularSTAT3 protein, humanSTAT3 Transcription FactorThiolester HydrolasesUsp30 protein, humanCirc-HSP90ANon-small cell lung cancerPD-1/PD-L1STAT3

Identifiers

PMID35750765
PMCPMC10992527
OpenAlexW4283377845

What OpenQuestion holds

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Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.